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Objective: To evaluate the efficacy and tolerability of anti-tumour necrosis factor a (TNFa) monoclonal antibody (infliximab) in the treatment of spondyloarthropathy (SpA) associated with active and inactive Crohn's disease (CD). Methods: Twenty four patients with SpA associated with active or inactive CD (16 active, 8 quiescent) were treated with anti-TNFa monoclonal antibody (infliximab) with repeated infusions for a period of 12-18 months. The treatment aimed at ameliorating the general musculoskeletal and spinal pain, controlling peripheral arthritis and enthesitis, decreasing the BASDAI score, modifying acute phase reactants, and reducing CD activity. Results: Infliximab improved both gastrointestinal (p,0.01) and overall articular symptoms (BASDAI, p,0.01; general musculoskeletal and spinal pain, p,0.01; peripheral arthritis, p,0.01) in patients with active CD. Additionally, infliximab effectively controlled not only axial involvement and peripheral arthritis but also enthesitis (p,0.01) and prevented inflammatory bowel disease reactivation in patients with inactive CD and low inflammatory markers. Amelioration of gut and musculoskeletal involvement persisted for up to 12 months. Conclusion: Infliximab may act on the inflammation of entheses and of periarticular structures, which usually does not cause a change in the haematological markers that are the main indicators of pain and joint ankylosis in SpA. Infliximab induces and maintains remission of CD while at the same time treating active and severe SpA, suggesting that it should be the preferred drug for the treatment of active and severe SpA associated with active or quiescent CD.

This study evaluated whether a new generation antioxidant Activin derived from the grape seed proanthocyanidins, could reduce the induction of the adhesion molecules as a result of inflammatory response in the plasma of systemic sclerosis (SSc) patients. SSc patients were divided into two groups: one group was treated with Activin, a grape seed-derived proanthocyanidins, while the other group served as control. Patients were given Activin 100 mg/day orally for one month after which the blood samples were withdrawn from both groups of the patients. Blood was also taken from normal human volunteers. Plasma was obtained in fasting state between 8 to 9 A.M. from two groups of SSc patients and controls. Soluble adhesion molecules including ICAM-1, VCAM-1, E-selectin and P-selectin as well as malonaldehyde, a marker for oxidative stress, were measured. The results of our study demonstrated up-regulation of these soluble adhesion molecules except for P-selectin, in the plasma of the SSc patients compared to those obtained from human volunteers. Activin significantly attenuated the increased expression of these adhesion molecules. In addition, there was a significant increase in the amount of malondialdehyde formation in the plasma of the SSc patients, which was also attenuated by Activin. The results of this study demonstrated that Activin could reduce the inflammatory response and the oxidative stress developed in SSc patients.

Objective. To evaluate health-related quality of life (HRQOL) in patients with systemic sclerosis (SSc) using the Short Form 36 (SF-36) and to correlate SF-36 scores with clinical and biologic markers. Methods. The SF-36 was administered to 24 controls and 24 SSc patients. SSc patients also were evaluated for subset (limited SSc [lSSc] and diffuse SSc [dSSc]), age, disease duration, angiotensin-converting enzyme (ACE) levels, autoantibodies, and skin and internal organ involvement. Results. The physical summary score (PSS) was lower in SSc patients than in controls (P < 0.05), whereas the mental summary score (MSS) was higher in dSSc than in lSSc patients (P < 0.05). Five of 8 single SF-36 domain scores were lower in SSc patients than in controls (P < 0.05). Vitality was higher in dSSc than in controls (P < 0.001). In SSc, elder age correlated with lower PSS; low ACE levels and high skin score correlated with higher general mental health and role limitations due to physical problems, respectively (P < 0.05). Patients with heart involvement had higher scores in general health perceptions (P < 0.05). Conclusion. The SF-36 shows that HRQOL is impaired in patients with SSc. Higher scores in MSS and vitality in patients with dSSc and correlations of high SF-36 scores with specific organ involvement suggest that SSc patients with severe disease are more able to cope with HRQOL modification.

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This study was conducted to assess ultrasound (US) and clinical changes of Baker's cyst (BC) of patients with knee osteoarthritis (OA) after steroid injection. Patients with knee OA complicated with symptomatic BC (40) were treated with US-guided direct (posterior) aspiration. The injection of 40 mg triamcynolone acetonide was in 20 patients direct into the BC and in other 20 subjects intra-articular (anterior). BC diameters (longitudinal, transverse, and thickness) were measured and followed up with US at baseline, 2, 4, and 8 weeks after injection. Swelling, pain, and range motion were scored at clinical examination with Rauschning and Lindgren classification (RLC, since 0 normal to 3 maximal signs). All US measures of BC and RLC significantly decreased after treatment, in comparison to baseline (p < 0.001) and during the follow-up, did not change through the time (no significant difference between 2, 4, and 8 weeks). At 4 and 8 weeks, diameters measured at US are lower when BC is directly infiltrated in comparison to intra-articular injection (p < 0.01). US steroid direct injection reduces US measures and clinics of BC in knee OA, in particular, when steroid is directly infiltrated into BC.

Lung macrophages may play a relevant role in oxidative processes producing both superoxide anion ðO À 2 Þ and NO. In this view, an antioxidant therapy can be useful in the treatment of systemic sclerosis (SSc) patients. N-Acetylcysteine (NAC) is able to expand natural antioxidant defenses by increasing intracellular gluthatione concentration and it has been proposed as an antioxidant therapy in respiratory distress syndromes. The aim of our study was to determine whether lung macrophages obtained from SSc patient bronchoalveolar lavage (BAL) express the inducible form of nitric oxide synthase (iNOS) and whether NAC can reduce the peroxynitrite ðONOO À Þ and O À 2 production of these cells. Alveolar macrophages were isolated from BAL of 32 patients and used for the immunocytochemical determination of iNOS, and the production of ONOO À and O À 2 was measured by fluorimetric or spectrophotometric methods, respectively. Lung macrophages obtained from SSc patients expressed a higher level of iNOS compared to healthy subject cells. NAC preincubation (5 Â 10 À5 M, 24 h) significantly reduced ()21%) the ONOO À production in formyl Met-Leu-Phe (fMLP)-activated cells and slightly reduced it under resting conditions, whereas NAC preincubation was unable to modify the release of O À 2 both in basal condition and in fMLP-stimulated cells. We conclude that since SSc lung macrophages express high levels of iNOS and produce a significant quantity of ONOO À , NAC administration reduces ONOO À production and can be an useful treatment to alleviate SSc symptoms. Ó 2002 Elsevier Science (USA). All rights reserved.Keywords: Systemic sclerosis; Inducible nitric oxide synthase; N-acetylcysteine; Peroxynitrite; Superoxide anion; Alveolar macrophages Nitric oxide (NO) 1 is physiologically produced by constitutive nitric oxide synthase isoforms (cNOS) and in several pathophysiological conditions by an inducible nitric oxide synthase isoform (iNOS). In systemic sclerosis (SSc) patients, NO is increased in exhaled air [1,2] while it is decreased in those patients with pulmonary hypertension [2,3]. Moreover, serum NO levels are enhanced [4], iNOS is highly expressed in mononuclear cells infiltrating the skin [4] and peripheral blood mononuclear cells produce increased NO levels when stimulated with IL-1 [5]. NO can be synthesized by different kinds of cells. Among these cells, macrophages play a pivotal role in the inflammatory infiltrate and, in patients with tubercolosis, iNOS is expressed in alveolar macrophages [6]. Inflammatory cells produce reactive oxygen species (ROS) that, reacting with NO, form tissue-damaging NO-derived inflammatory oxidants. ROS